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Biomedical subjects

F J Dixon

Publications and source records attributed to F J Dixon.

At least 19 recordsLinked to original sources
PubMed1979

Association of circulating retroviral gp70-anti-gp70 immune complexes with murine systemic lupus erythematosus.

Endogenous retroviral gp70 was investigated as a participant in the pathogenesis of a lupus-like disease that spontaneously develops in four kinds of mice (NZB, NZB x W MRL/1, and male BXSB). Sera from these strains contain a heavy form of gp 70 that varies in sedimentation rates from 9S to 19S in sucrose density gradient analysis and appears with the onset of disease and persists throughout its course. Immunologically normal strains of mice do not develop rapidly sedimenting gp70 by 8-10 mo of life. The fact that the heavy gp70 is selectively absorbed with anti-IgG antibodies or with Staphylococcus aureus protein A suggests that it is complexed with antibodies. The incidence and quantities of these gp70 ICs rise with the progression of disease in all strains with lupus. These findings suggest that Ig-complexed heavy gp70 may be involved in the pathogenesis of glomerulonephritis of mice with SLE.

Animals↗
PubMed1979

Distribution of lymphocytes identified by surface markers in murine strains with systemic lupus erythematosus-like syndromes.

The frequencies and absolute numbers of B and T cells in the lymphoid organs of five murine strains (NZB, (NZB X NZW)F1, BXSB, MRL/l, and MRL/n) with SLE-like syndromes were examined. We assessed the frequencies of cells bearing surface Ig, C3d and IgG Fc receptors, and theta-antigen. The sequential expression of Ig isotopes on developing B cells and the Ig isotypes expressed on adult B cells were ascertained. In addition, the Ly subsets and the expression of Ia antigens coded for by the I-J subregion of the mouse H-2 complex were examined. Compared to normal, older mice, New Zealand mice had low frequencies and absolute numbers of B cells, BXSB mice had a moderate B-cell proliferation, and MRL/l mice had normal absolute numbers of B cells but a reduced frequency concomitant with a massive T-cell proliferation. Old New Zealand mice and BXSB mice had reduced frequencies and absolute numbers of T cells compared to old controls. The developmental Ig-isotype diversity during the 1st wk of age was similar in normal mice and those with autoimmune manifestations. Mature B cells were present in lymphoid organs of New Zealand mice and BXSB mice as evidenced by the high frequency of C3d receptor-bearing cells and Ig-isotype expression (high ratio of IgM- to IgD-bearing cells) in adult spleen cells. Numbers of IgG Fc receptor-bearing cells were reduced in autoimmune mice with advanced age and disease. The proliferating T cells in MRL/l mice were found to be theta-antigen positive but Ly null. These theta+-, Ly null cells may have arisen from Ly123+ T cells. MRL/l and BXSB mice seemed normal in their content of T cells bearing Ia antigens coded for by the I-J subregion of H-2. Overall, mice with autoimmune manifestations appear to express perturbations in T and B cells with development of disease, and their patterns of change vary from one strain to another.

Aging↗
PubMed1979

Serum-serum interactions in autoimmune mice.

Sera from a majority of old, sick mice of the MRL/l strain interact with other MRL/l sera to form visible immunoprecipitates and fix complement. The mouse sera can be divided into two sets such that interset interactions are far more common than intraset ones. The reactive principle in each mouse serum is IgG in the form of an intermediate-sized complex. Reactivity between sera is dependent on IgG anti-IgG specificities.

Animals↗
PubMed1979

Use of circulating immune complex levels in the serodifferentiation of endocarditic and nonendocarditic septicemias.

Distinguishing endocarditic from nonendocarditic septicemias is prognostically and therapeutically important. One hundred two patients with both valvular and nonvalvular sepsis were studied for the presence and quantitation of circulating immune complexes. Ninety per cent of the patients with infective endocarditis versus 50 per cent of septic patients without infective endocarditis had circulating immune complex levels (p less than 0.005). Mean circulating immune complex levels in patients with infective endocarditis were significantly higher than in those without infective endocarditis, 106 +/- 18.58 microgram/ml versus 31 +/- 7.4 microgram/ml (p less than 0.005). Only three of 52 patients without infective endocarditis had circulating immune complex levels greater than 100 microgram/ml, as opposed to 16 of 50 patients with infective endocarditis (p less than 0.005). Similarly, one of 52 patients without infective endocarditis has circulating immune complex levels greater than 200 microgram/ml, as opposed to eight of 50 patients with infective endocarditis (p less than 0.05). In 92 per cent of the patients without infective endocarditis and 76 per cent of those with infective endocarditis peak circulating immune complex levels developed within 14 days after their entry into the study, often on the initial sampling. In febrile, septicemic patients with clinical symdromes nonclassic for endocarditis, measurements of serial circulating immune complex levels may be of adjunctive diagnosis importance. If circulating immune complex levels are undetectable, endocarditis would appear less likely; alternatively, levels above 100 to 200 microgram/ml would suggest a valvular rather than nonvalvular septic focus.

Antigen-Antibody Complex↗
PubMed1979

Immunologic mechanisms in nephritogenesis.

At least two different immunopathologic pathways that together account for most clinical nephritis have been delineated. Most common is the situation in which antigen-antibody complexes form in the circulation and lodge in renal basement membranes. The second involves antibodies to specific kidney structures. Both may initiate inflammatory injuries that adversely alter glomerular and tubular function.

Antibodies↗
PubMed1979

Circulating immune complexes in experimental streptococcal endocarditis: a monitor of therapeutic efficacy.

An important problem in the management of infective endocarditis has been the delineation of laboratory procedures that are sensitive, reliable indicators of therapeutic efficacy. Because circulating, complement-containing immune complexes of the IgG type (CICs) have been demonstrated in most humans with infective endocarditis, serum CIC levels during the natural course of the infection and in response to penicillin therapy were studied in 42 rabbits with right-sided endocarditis due to Streptococcus salivarius. A significant rise in the level of CICs in both 21 control rabbits and 21 treated rabbits was observed after induction but before treatment of infective endocarditis (P less than 0.01). In the 17 successfully treated rabbits, CIC levels fell sharply during the first week of therapy and remained at preinduction levels thereafter (P less than 0.005). In contrast, CIC values did not change significantly either in control animals or in the four treated animals with refractory endocarditis, although in the latter animals, serum bactericidal titers remained less than or equal to 1:32. These findings suggest that serial measurements of CIC levels during antimicrobial therapy of infective endocarditis may aid in monitoring therapeutic efficacy.

Animals↗
PubMed1979

T cell-mediated immune responses of lupus-prone BXSB mice and other murine strains.

Cellular-mediated immunity in the newly described BXSB strain of mice, which is prone to autoimmune disease, has been compared with that of two other strains, C57Bl/6 and 129/J. Quantificaiton of cytotoxic T cell responses to alloantigens and viruses (lymphocytic choriomeningitis and vaccinia virus) showed no difference in the kinetics of appearance and relative activity of cytotoxic T cells per spleen between the young and old BXSB and the control mice. The T cell-dependent primary footpad swelling after local injection with lymphocytic choriomeningitis virus was within the same range for all strains tested with respect to kinetics, but the size was greater by two-fold in C57Bl/6 mice. The susceptibility to systemic infection and subsequent induction of lymphocytes immune to Listeria monocytogenes were about equivalent in all strains. However, clearance of Listeria by the reticuloendothelial system and early non-immune bactericidal activity of the young and old BXSB were significantly lower than in the control strains. The results indicate that the cellular-mediated immunity (CMI) of BXSB mice compared favourably with that of other strains and that there is no apparent differences between CMI of BXSB mice before the onset of disease and during the course of disease. The role of the reduced reticuloendothelial function of BXSB mice in their autoimmune disease or in their high susceptibility to infection remains to be determined.

Animals↗
PubMed1979

Natural thymocytotoxic autoantibodies in autoimmune and normal mice.

Natural thymocytotoxic autoantibodies (NTA) were found in all mouse strains. Among those strains that show autoimmune syndromes resembling human systemic lupus erythematosus (SLE), the NZB and NZBxNZW had high levels of NTA, the BXSB had moderate levels, and the MRL/1 and MRL/n had very low levels. In addition, some normal strains had high levels, sometimes even higher than the autoimmune strains. The NTA were mostly IgM and were present, but not concentrated, in the cryoprecipitates of teh autoimmune mouse strains. In most strains, they were directed toward an antigen shared by thymocytes and brain. The failure to find high levels of NTA in all autoimmune mouse strains, as well as the finding of very high levels in some normal strains, make it unlikely that such auto-antibodies are a fundametnal etiologic factor in all murine SLE.

Absorption↗
PubMed1979

IgM rheumatoid factors in mice injected with bacterial lipopolysaccharides.

Bacterial lipopolysaccharides (LPS) induced the formation of IgM rheumatoid factors (RF) in several strains of mice including athymic C57BL/6 nude mice, but not in the LPS-resistant C3H/HeJ mice. The RF induced by LPS reacted not only with murine IgG but also with IgG from cows, goats, guinea pigs, and humans. The kinetics of this RF response to injection of LPS were similar to those of antibody response against DNA and a hapten, dinitrophenyl (DNP), and to those of total IgM production. In addition, the RF activity of individual serum samples correlated significantly with levels of anti-DNA and anti-DNP antibodies and of IgM. Therefore, it is concluded that the induction of RF results from polyclonal antibody synthesis by B cells stimulated with LPS. This observation suggests that LPS or LPS-like substances may help to generate RF in patients with rheumatoid arthritis or with some infectious diseases.

Animals↗
PubMed1979

Degenerative vascular disease and myocardial infarction in mice with lupus-like syndrome.

The pathogenesis of the degenerative vascular disease and myocardial infarction that develop in mice with lupus-like disease was studied by immunofluorescence, light microscopy, and electron microscopy. Medium and small coronary arteries and arterioles of both infarcted and noninfarcted hearts had focal degenerative lesions consisting of deposits of periodic-acid--Schiff (PAS)-positive or eosinophilic material in the intima and to a lesser extent in the media, degenerative changes in the media without accompanying cellular inflammation, and occasional proliferation or swelling of intimal cells. These lesions often narrowed and, together with platelet aggregation, occasionally occluded the vascular lumens. Granular deposits of mouse immunoglobulin, C3, and occasionally gp70 were present in the walls of medium and small arteries, arterioles, and venules of both infarcted and noninfarcted myocardium. Dense deposits of foreign material were found by electron microscopy in areas corresponding to the immune deposits. These findings are consistent with the interpretation that these noninflammatory vascular lesions are caused by local deposition of antigen--antibody complexes. The immune-complex--mediated injury appears to lead to thrombotic and/or obliterative vascular changes that contribute to decrease of the coronary blood flow and to the development of myocardial infarction.

Animals↗
PubMed1979

Chemically induced bidirectional differentiation of embryonal carcinoma cells in vitro.

N,N-dimethylacetamide, hexamethylene bisacetamide, and Polybrene induced rapid and extensive differentiation in vitro in an otherwise slowly differentiating subline of embryonal carcinoma cells. The type of differentiated cell induced was dependent on the spatial organization of the stem cells during drug treatment. In monalayer culture "epithelial" cells were produced exclusively. However, treatment of aggregated suspension cultures yielded predominantly "fibroblast-like" cells. The undifferentiated embryonal carcinoma cells and the two differentiated cell types were morphologically distinct when examined by light microscopy, scanning electron microscopy, and transmission electron microscopy; and they had differences in cell surface antigens. Both differential cell types produced large amounts of fibronectin, whereas the embryonal carcinoma cells produced only minimal amounts. This system provides a convenient way to induce relatively synchronous differentiation of embryonal carcinoma cells into specific differentiated cell types.

Acetamides↗
PubMed1979

The activation of the alternative complement pathway by fetal calf serum and mouse thymocytes.

Mouse thymocytes activated the alternative complement pathway of mouse serum in the presence of heated fetal calf serum. The activation required C3 from the fetal calf serum but was independent of antibody either in the murine or bovine serum. No other murine cells tested, including erythrocytes, peripheral blood lymphocytes, lymph node cells, spleen cells, and various cultured cell lines, activated the alternative complement pathway as effectively as thymocytes. In addition, sera from species other than cows could not substitute for fetal calf serum. The C3 deposited on thymocytes was in the form of both C3b (immune adherence positive) and C3bi (conglutinable). We propose that the basis of activation in this system is the specific protection of bovine C3b on mouse thymocyte surface.

Absorption↗